MiR-7 Triggers Cell Cycle Arrest at the G1/S Transition by Targeting Multiple Genes Including Skp2 and Psme3

Sánchez, Nilda; Gallagher, Mary E.; Lao, Nga T.; Gallagher, Clair; Clarke, Colin; Doolan, Padraig; Aherne, Sinéad; Blanco, Alfonso; Meleady, Paula; Clynes, Martin; Barron, Niall

doi:10.1371/journal.pone.0065671

Cited by 56 publications

(45 citation statements)

References 60 publications

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“…In this study, we further confirmed the oncogenic potential of miR-7 through its association with the chromatin remodeling factors SMARCD1 and p53, thereby influencing anticancer drug resistance. miR-7 was recently reported to have dual functions in both cell cycle arrest and anti-apoptosis in CHO cells (29). miR-7 indirectly down-regulated p53 expression and activated p-Akt in CHO cells to protect cells from apoptosis, indicating that miR-7 plays an elegant role in fine-tuning cell cycle regulation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-7 Compromises p53 Protein-dependent Apoptosis by Controlling the Expression of the Chromatin Remodeling Factor SMARCD1

Hong¹,

Lin²,

Chou³

et al. 2016

Journal of Biological Chemistry

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We previously demonstrated that the epidermal growth factor receptor (EGFR) up-regulated miR-7 to promote tumor growth during lung cancer oncogenesis. Several lines of evidence have suggested that alterations in chromatin remodeling components contribute to cancer initiation and progression. In this study, we identified SMARCD1 (SWI/SNF-related, matrixassociated, actin-dependent regulator of chromatin, subfamily d, member 1) as a novel target gene of miR-7. miR-7 expression reduced SMARCD1 protein expression in lung cancer cell lines. We used luciferase reporters carrying wild type or mutated 3UTR of SMARCD1 and found that miR-7 blocked SMARCD1 expression by binding to two seed regions in the 3UTR of SMARCD1 and down-regulated SMARCD1 mRNA expression. Additionally, upon chemotherapy drug treatment, miR-7 downregulated p53-dependent apoptosis-related gene BAX (BCL2-associated X protein) and p21 expression by interfering with the interaction between SMARCD1 and p53, thereby reducing caspase3 cleavage and the downstream apoptosis cascades. We found that although SMARCD1 sensitized lung cancer cells to chemotherapy drug-induced apoptosis, miR-7 enhanced the drug resistance potential of lung cancer cells against chemotherapy drugs. SMARCD1 was down-regulated in patients with non-small cell lung cancer and lung adenocarcinoma cell lines, and SMARCD1 and miR-7 expression levels were negatively correlated in clinical samples. Our investigation into the involvement of the EGFR-regulated microRNA pathway in the SWI/ SNF chromatin remodeling complex suggests that EGFRmediated miR-7 suppresses the coupling of the chromatin remodeling factor SMARCD1 with p53, resulting in increased chemo-resistance of lung cancer cells.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-7 Compromises p53 Protein-dependent Apoptosis by Controlling the Expression of the Chromatin Remodeling Factor SMARCD1

Hong¹,

Lin²,

Chou³

et al. 2016

Journal of Biological Chemistry

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“…6D). In fact, REGγ is reported to be regulated by other signals than mutant p53, the most studied is miR-7 [56][57][58], a tumor suppressor in many cancers. Therefore we suppose REGγ could be upregulated by some undetermined molecules in these p53-negative specimens and cells.…”

Section: Discussionmentioning

confidence: 99%

Mutant p53 (p53-R248Q) functions as an oncogene in promoting endometrial cancer by up-regulating REGγ

et al. 2015

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“…FBXW11 was regulated by miR-106b-25 cluster and involved in tumor invasion and metastasis [37]. SKP2 was regulated by miR-7 [38]. We then asked whether FBXO31 was regulated by miRNAs.…”

Section: Discussionmentioning

confidence: 99%

F-box protein FBXO31 is down-regulated in gastric cancer and negatively regulated by miR-17 and miR-20a

Zhang

Kong

et al. 2014

Oncotarget

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FBXO31, a subunit of the SCF ubiquitin ligase, played a crucial role in neuronal development, DNA damage response and tumorigenesis. Here, we investigated the expression and prognosis value of FBXO31 in human primary gastric cancer (GC) samples. Meanwhile, the biological role and the regulation mechanism of FBXO31 were evaluated. We found that FBXO31 mRNA and protein was decreased dramatically in the GC tissue compared with the adjacent non-cancerous tissues. FBXO31 expression was significantly associated with tumor size, tumor infiltration, clinical grade and patients' prognosis. FBXO31 overexpression significantly decreased colony formation and induced a G1-phase arrest and inhibited the expression of CyclinD1 protein in GC cells. Further evidence was obtained from knockdown of FBXO31. Ectopic expression of FBXO31 dramatically inhibited xenograft tumor growth in nude mice. miR-20a and miR-17 mimics inhibited, whereas the inhibitor of miR-20a and miR-17 increased, the expression of FBXO31, respectively. miR-20a and miR-17 directly bind to the 3'-UTR of FBXO31. The level of miR-20a and miR-17 in GC tissue was significantly higher than that in surrounding normal mucosa. Moreover, a highly significant negative correlation between miR-20a (miR-17) and FBXO31 was observed in these GC samples. Therefore, effective therapy targeting the miR-20a (miR-17)-FBXO31-CyclinD1 pathway may help control GC progression.

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MiR-7 Triggers Cell Cycle Arrest at the G1/S Transition by Targeting Multiple Genes Including Skp2 and Psme3

Cited by 56 publications

References 60 publications

MicroRNA-7 Compromises p53 Protein-dependent Apoptosis by Controlling the Expression of the Chromatin Remodeling Factor SMARCD1

MicroRNA-7 Compromises p53 Protein-dependent Apoptosis by Controlling the Expression of the Chromatin Remodeling Factor SMARCD1

Mutant p53 (p53-R248Q) functions as an oncogene in promoting endometrial cancer by up-regulating REGγ

F-box protein FBXO31 is down-regulated in gastric cancer and negatively regulated by miR-17 and miR-20a

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